Fish Physiology and Biochemistry最新文献

Low dissolved oxygen (DO), or hypoxia, has a profound impact on the physiological and neurological health of aquatic organisms, particularly oxygen-sensitive organs such as the brain. The aim was to investigate the effects of pyrimidine and its derivative, arylvinylpyrimidine (AVP), on neuronal health in the brain of the lesser studied Heteropneustes fossilis under hypoxic conditions. Laboratory-acclimatized fish were exposed to critical threshold hypoxia (2 mg/L DO for 8 h) based on behavioural and brain histopathology observations. For remediation by pyrimidine and AVP in the hypoxic brain, fish were divided into eight experimental groups; four groups maintained for five days as control [without treatment, with 8 h hypoxia, and only drug effect (pyrimidine, 10 pg/mL or AVP, 0.1 µg/mL)] and four groups were maintained as pre- (drug for five days followed by hypoxia for 8 h) and post- (8 h hypoxia followed by drug for five days) treatment with pyrimidine (10 pg/mL) and AVP (0.1 µg/mL) separately. The results showed that air breather H. fossilis exhibited severe hypoxic effects on neuronal health. Hypoxia significantly elevated antioxidant enzyme activity, and lipid peroxidation (LPO), reduced carbohydrate concentration, and increased total lipid content without affecting total protein level in the brain. The hypoxic brain showed a clear stress effect on cellular and neuronal texture. Hypoxia also significantly influenced neurotransmitter synthesis enzymes [acetylcholinesterase (AChE), tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DBH), and tryptophan hydroxylase-2 (TPH2)]. Hypoxia induced brain alteration was effectively reversed by pyrimidine and AVP treatment. Among different experimental sets, post-treatment being more effective than pre-treatment, and AVP showed greater effectiveness than pyrimidine. These findings demonstrate pyrimidine and AVP as neuroprotective agents against hypoxia-induced damage in the H. fossilis brain and suggest their potential therapeutic utility in managing hypoxia induced neuronal damage in aquatic animals.

Megalobrama amblycephala is a key freshwater fish species in Chinese aquaculture, valued for its high artificial propagation success and relative resistance to common aquaculture diseases. However, it is sensitive to hypoxia, and its molecular responses to hypoxic stress in the heart remain relatively unknown. Herein, we investigated the effects of hypoxia on myocardial enzyme activities (creatine kinase, creatine kinase myocardial band isoenzyme, lactate dehydrogenase, and α-hydroxybutyrate dehydrogenase), histological structure, and transcriptome changes in the heart of M. amblycephala. The fish were divided into five groups, including normoxia control (N0), hypoxia for 6, 12, and 24 h (H6, H12, and H24, respectively), and reoxygenation for 24 h (R24) groups. The results showed that hypoxia significantly increased myocardial enzyme activities. Histological analysis revealed that hypoxia induced slight swelling and disorganization of myocardial fibers, while reoxygenation partially restored their structural integrity. Transcriptome sequencing identified 4,269 DEGs, with 964, 1,159, 812, and 1,334 identified in the H6, H12, H24, and R24 groups, respectively, compared to the N0 group. KEGG pathway analysis identified circadian rhythm, cardiac muscle contraction, fatty acid degradation, hypertrophic cardiomyopathy, and fluid shear stress and atherosclerosis pathways as candidate molecular pathways involved in hypoxia tolerance. Notably, several key genes, including cry5, LOC125248347, cacng5b, atp2a1l, LOC125252961, aldh3a1, gcdha, edn1, atp2a1, gpc1a, and hsp90aa1.2, were significantly up-regulated in the H24 group, highlighting their potential roles in the adaptive responses to hypoxic stress. These findings provide new insights into the physiological, histological, and molecular responses underlying hypoxia adaptation in M. amblycephala, laying the groundwork for future studies on hypoxia-related molecular mechanisms in other economically important fish species.

Understanding individual variability in stress physiology is critical for improving fish welfare and optimizing production in aquaculture. This study investigates the variability of cortisol responses to acute stress in juvenile greater amberjack (Seriola dumerili), a species of increasing interest in Mediterranean aquaculture. It also examines whether early-life thermal exposure and individual behavioral coping styles, particularly risk-taking behavior, are associated with divergent cortisol responsiveness. Juvenile amberjacks were reared under controlled conditions and assessed for risk-taking behavior using a standardized group-based behavioral test. Acute stress responses were evaluated by measuring physiological stress indicators over time, focusing on cortisol dynamics to assess both inter-individual variability and intra-individual consistency. Results demonstrate that cortisol responsiveness is a repeatable and stable individual trait in this species, showing no significant association with early thermal conditions or behavioral profiles. While early-life temperature influenced risk-taking behavior in one experimental trial, this trait did not correlate with variability in growth or physiological stress markers. Overall, this study shows that cortisol responsiveness in juvenile greater amberjack is a repeatable individual trait, not being affected by the examined early-life temperature exposure and intrinsic risk-taking behavior, highlighting the significance of individual variability for understanding stress physiology in aquaculture.

This study aims to investigate the ameliorative effects of fermented Chinese herbal medicine (FCHM) on manganese (Mn)-induced growth inhibition and liver damage in largemouth bass. The experiment was set up with eight groups: Mn (0, 0.750, 1.125, and 1.688 mg/L) and Mn + FCHM (0, 0.750, 1.125, and 1.688 mg/L). Among these, the Mn (0 mg/L) group served as the control group. The Mn groups were fed a basal diet, while the Mn + FCHM groups were fed a diet containing 1% FCHM. The experiment lasted for 60 days. The results indicated that Mn exposure reduced growth performance and induced Mn accumulation in the liver, tissue structural damage, oxidative stress, and inflammation. One percent FCHM partially restored growth performance, increased the activity and gene expression of GSH-PX, CAT, and SOD enzymes in the liver, reduced MDA and Mn content, increased the expression of anti-inflammatory markers IL-10 and TGF-β1 mRNA, decreased the expression of IL-15, IL-8, IL-1β, and TNF-α mRNA, and alleviated liver tissue pathological damage. In summary, this study found that FCHM can improve the antioxidant capacity of largemouth bass, alleviate Mn-induced liver inflammatory damage, and thereby enhance the growth performance of largemouth bass.

Cytochrome P450 aromatase, the product of the CYP19A1 gene, is a key enzyme in estrogen biosynthesis. Most teleost fish have two distinct isoforms of aromatase, ovarian aromatase (AroA) and brain aromatase (AroB) encoded by cyp19a1a and cyp19a1b, respectively. Although aromatase is expressed in the brain across vertebrates, it is present at uniquely high levels in teleost fish, where its role in brain development is not fully understood. Therefore, in this study, the effects of exposure to fadrozole (Fad), an aromatase inhibitor, and knockdown of the AroB gene by using a morpholino antisense oligonucleotide (MO) on the expression of dopaminergic (DAergic) neurons were investigated in zebrafish embryos and larvae. Fad exposure decreased the expression of tyrosine hydroxylase (TH) as detected by immunostaining at 48 h post fertilization (hpf) and impaired locomotor activities including tactile response at 72 hpf and swimming distance at 6 days post fertilization (dpf), which was reversed by the addition of 17β-estradiol (E₂). Additionally, in real-time PCR analysis, Fad exposure significantly reduced the gene expression of TH (th1 and th2), AroB, and estrogen receptors (esr2a and esr2b), whereas the expression of another estrogen receptor gene, esr1, and the AroA gene remained unchanged. Similarly, AroB-MO injection decreased immunostained TH expression, which was rescued by co-injection with AroB mRNA or the addition of E_2. AroB-MO injection reduced locomotor activity, which was partially restored by the addition of E₂ or L-dopa. In conclusion, the results indicate that brain-formed estrogen plays a significant role in the maintenance of DAergic neurons in the early development of zebrafish.

This study aimed to evaluate the inclusion of ora-pro-nobis (OPN) flour in tilapia diets (0%, 5%, 10%, and 15%) and its influence on zootechnical performance, digestive processes, metabolism, antioxidant status, and meat proximate composition. The 5% inclusion level improved zootechnical parameters compared to the control. Moreover, the activities of the digestive enzymes chymotrypsin, trypsin, lipase, amylase, and maltase increased with OPN supplementation. The fillet proximate composition showed higher protein content across all supplemented groups, along with an increase in lipid content in the 5% group. The fatty acid profile of the fillets revealed a predominance of unsaturated fatty acids, with a dose-dependent increase in polyunsaturated fatty acids (PUFAs) at 5%, 10%, and 15%, and an increase in long-chain PUFAs observed in the 5% and 10% groups. Blood biochemical parameters (glucose, cholesterol, triglycerides, albumin, ALT, AST, alkaline phosphatase, lactate dehydrogenase, total proteins, and urea) were not affected by OPN supplementation. However, higher inclusion levels (10% and 15%) increased in the hepatic activities of AST, ALT, glutamate dehydrogenase (GLDH), and fatty acid synthase (FAS), while decreasing the activities of hexokinase (HK), phosphofructokinase-1 (PFK), and glucose-6-phosphate-dehydrogenase (G6PDH). No changes were observed in the hepatic activities of citrate synthase (CS), malate dehydrogenase (MDH), NADH dehydrogenase, or β-hydroxyacyl-CoA dehydrogenase (HOAD). Under transport stress challenge, all experimental groups showed improved survival rates, with no changes in hepatic catalase and glutathione reductase (GR) activity nor in lipid peroxidation levels. However, there were reductions in glutathione peroxidase (GPx) activity and glutathione (GSH) content. The observed effects on performance, metabolism, and stress resistance highlight the potential of OPN as a modulator of metabolic and antioxidant status in fish. These findings suggest that OPN flour can be a valuable supplement for tilapia diets when used at inclusion levels below 10%.

Aquatic habitats that include antibiotic residues pose the risk of causing antibiotic resistance as well as negative health impacts on human and non-target species. To assess the effects of enrofloxacin at environmentally relevant concentrations on Oreochromis niloticus, growth performance of O. niloticus, oxidative stress, and the transcriptional gene expressions of apoptotic enzymes and pro-inflammatory cytokines were determined in the gills. Environmentally relevant concentrations of enrofloxacin (1-10-100 µg/L) were exposed to fish for periods of 7 days and 21 days. The results demonstrated that enrofloxacin negatively affected growth performance at high applied concentrations in O. niloticus in the long-term effect. Furthermore, enrofloxacin disrupts the GSH-dependent antioxidant system in the gills, leading to oxidative stress through increased lipid peroxidation. Short-term exposure to low and medium concentrations of enrofloxacin increased the mRNA expression of apoptotic enzymes (caspase-3, caspase-8) and pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) in the gills. Considering the research findings, environmentally relevant concentrations of enrofloxacin negatively impact growth performance in O. niloticus and induce toxicity through the induction of inflammation and apoptosis, coupled with oxidative stress in the gills. In conclusion, the ecotoxicological impact of enrofloxacin necessitates careful consideration due to its potential to negatively affect non-target organisms.

Arsenic (As) is a widespread environmental pollutant that poses serious risks to aquatic organisms, particularly affecting neurological health through oxidative damage, endoplasmic reticulum (ER) stress, and apoptosis. Natural bioactive compounds such as genistein (GNT), a soy-derived isoflavone, have shown potential in counteracting heavy metal-induced toxicity due to their antioxidant and anti-apoptotic activities. This study evaluated the neuroprotective effects of dietary GNT (500 mg/kg) in Nile tilapia (Oreochromis niloticus) exposed to 10 µg/L As for 60 days. Arsenic exposure significantly impaired neurobehavioral performance, including reduced ingestive, swimming behaviors, and aggression. Dietary supplementation with GNT effectively ameliorated these behavioral disturbances. At the biochemical level, As exposure decreased the activities of key brain antioxidants, superoxide dismutase, catalase, and reduced glutathione, while increasing malondialdehyde (MDA). Genistein reversed these oxidative imbalances, restoring antioxidant enzyme activities and reducing MDA levels. Furthermore, GNT significantly upregulated brain acetylcholinesterase content and modulated the expression of genes associated with endoplasmic reticulum (ER) stress and apoptosis. Specifically, GNT reversed As-induced dysregulation in the expression of jnk, chop, eif-2a, xbp-1, ire-1a, atf-6, bip, perk, caspase-3, bax, and bcl-2, indicating its role in mitigating ER stress and apoptotic signaling. Histopathological examination confirmed the protective role of GNT against As-induced brain tissue damage. In conclusion, GNT supplementation offers promising neuroprotection against As-induced toxicity via the modulation of oxidative stress, ER stress, and apoptosis in Nile tilapia.

Climate change, including global warming, is associated with an increase in water temperature, which leads to increased water evaporation from water bodies, resulting in elevated salinity and decreased dissolved oxygen (DO₂) levels. This may deteriorate fish health and productivity, and threaten the sustainability of aquaculture. Hence, the current study was carried out to investigate the interactions between hypoxia and increased salinity, as well as their impact on growth parameters, digestive enzymes, serum biochemistry, antioxidative response, and histopathology in Nile tilapia (Oreochromis niloticus). A total of 270 juvenile fish were impartially allocated into 18 aquariums (six treatments with three replicates) in a 2 × 3 factorial design, which included two oxygen levels (normoxia = 5.5-6 mg/L DO₂ and hypoxia = 1-1.5 mg/L DO₂) and three salinity conditions (0, 7, and 14 g/L) over 56 days feeding on a commercial diet (32% protein). Salinity and hypoxia significantly reduced growth and feed utilization. The most declared weight gain and feed conversion ratios were obtained under normoxic and freshwater conditions, although the survival rate was not considerably altered. Hypoxia increased RBCs, hemoglobin, and hematocrit, while elevated salinity significantly reduced them. Hypoxia and elevated salinity impaired digestive enzymes (protease, lipase, α-amylase), increased plasma cortisol, glucose, and liver enzyme levels (aspartate aminotransferase and alanine aminotransferase), lipid profile levels (total cholesterol and triglycerides), while decreasing plasma total protein. The immunity response (lysozyme activity, respiratory burst, phagocytosis, and IgM) was markedly reduced under hypoxia and hypersalinity, while they were markedly enhanced under normoxia and freshwater conditions. Fish reared under hypoxia and higher salinity exhibited structural damage in gills, intestine, and liver tissues. Our findings show that environmental stressors (hypoxia and excessive salinity) harm Nile tilapia growth and well-being, emphasizing the need to improve aquaculture settings in response to climate change.